Tuesday, May 20, 2014

Fly study reports uncovering a nuclear role for FMRP.

Zhang W, Cheng Y, Li Y, Chen Z, Jin P, Chen D. A feed-forward mechanism involving Drosophila fragile X mental retardation protein triggers a replication stress-induced DNA damage response. Hum Mol Genet. 2014 May 15. pii: ddu241. PMID: 24833720.

From the abstract: "Fragile X syndrome, a common form of inherited mental retardation, is caused by loss of the fragile X mental retardation protein (FMRP). ... Here we show that Drosophila dFMR1 in nucleus is required for replication stress-induced H2Av phosphorylation in the DNA damage response (DDR). ..."

Saturday, May 10, 2014

Addressing metabolic issues in a fly model of Adenine Nuclear Translocase (ANT) insufficiency

Vartiainen S, Chen S, George J, Tuomela T, Luoto KR, O'Dell KM, Jacobs HT. Phenotypic rescue of a Drosophila model of mitochondrial ANT1 disease. Dis Model Mech. 2014 May 8. PMID: 24812436.

From the abstract: "... Our findings illustrate the potential of different therapeutic strategies for ANT-linked diseases, based on increasing mitochondrial bioenergy production, or on alleviating metabolic stress."

Thursday, May 8, 2014

Two papers--flies and neurodegenerative disease--including a fluorescent protein-based fly eye assay

There are more papers to catch up on but in the meantime, these caught my eye today:

Rumpf S, Bagley JA, Thompson-Peer KL, Zhu S, Gorczyca D, Beckstead RB, Jan LY, Jan YN. Drosophila Valosin-Containing Protein is required for dendrite pruning through a regulatory role in mRNA metabolism. Proc Natl Acad Sci U S A. 2014 May 5. PMID: 24799714.

Burr AA, Tsou WL, Ristic G, Todi SV. Using membrane-targeted green fluorescent protein to monitor neurotoxic protein-dependent degeneration of Drosophila Eyes. J Neurosci Res. 2014 May 2. PMID: 24798551. From the abstract: "Here, we describe a sensitive fluorescence-based method to observe, monitor, and quantify mild Drosophila eye degeneration caused by various proteins, including the polyglutamine disease proteins ataxin-3 (spinocerebellar ataxia type 3) and huntingtin (Huntington's disease), mutant α-synuclein (Parkinson's disease), and Aβ42 (Alzheimer's disease). We show that membrane-targeted green fluorescent protein reports degeneration robustly and quantitatively. This simple yet powerful technique, which is amenable to large-scale screens, can help accelerate studies to understand age-related degeneration and to find factors that suppress it for therapeutic purposes."